Evidence map›Paper›PMID 29504068›Full record

ArticleInvestigational new drugs2018

Histone deacetylase inhibitor chidamide induces growth inhibition and apoptosis in NK/T lymphoma cells through ATM-Chk2-p53-p21 signalling pathway.

Jianan Zhou, Canjing Zhang, Xianxian Sui, Shengxuan Cao, Feng Tang, Shuhui Sun, Songmei Wang, Bobin Chen

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Article in Investigational new drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jianan ZhouDepartment of Hematology, Huashan Hospital, Shanghai Medical College, Fudan University, 12 Urumqi Middle Road, Shanghai, 200040, China.
Canjing ZhangInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Xianxian SuiLaboratory of Medical Molecular Biology, Experimental Teaching Center, School of Basic Medical Sciences, Fudan University, Dongan Road, Shanghai, 200032, China.
Shengxuan CaoShanghai Medical College, Fudan University, Shanghai, China.
Feng TangDepartment of Pathology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Shuhui SunKey Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Songmei WangLaboratory of Medical Molecular Biology, Experimental Teaching Center, School of Basic Medical Sciences, Fudan University, Dongan Road, Shanghai, 200032, China. smwang2@fudan.edu.cn.
Bobin ChenDepartment of Hematology, Huashan Hospital, Shanghai Medical College, Fudan University, 12 Urumqi Middle Road, Shanghai, 200040, China. bbchen@fudan.edu.cn.ORCID 0000-0002-1775-6221

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the anti-tumour effects and the underlying molecular mechanisms of a new oral histone deacetylase inhibitor (HDACi), chidamide, in NK/T cell lymphoma (NKTCL), a rare and highly aggressive non-Hodgkin lymphoma with poor outcomes. SNT-8 and SNK-10 NKTCL cell lines were exposed to different concentrations of chidamide for the indicated time. The treated cells were analysed for cell proliferation, cell cycle progression, and cell apoptosis. Proteins in the AKT/mTOR and MAPK signalling pathways and the DNA damage response (DDR) cell cycle checkpoint pathway were measured by Western blotting. Chidamide inhibited cell proliferation in a dose- and time-dependent manner, arrested cell cycle progression at the G0/G1 phase, and induced apoptosis in the NKTCL cell lines. In addition, we found that chidamide suppressed the phosphorylation levels of proteins in the AKT/mTOR and MAPK signalling pathways and activated the DDR cell cycle checkpoint pathway, that is, the ATM-Chk2-p53-p21 pathway. Expression of EBV genes was also assessed by Real-Time PCR. Chidamide induced EBV lytic-phase gene expression in EBV-positive NKTCL. Our results provide evidence that chidamide shows antitumour effects by inhibiting the AKT/mTOR and MAPK signalling pathways and activating the ATM-Chk2-p53-p21 signalling pathway in vitro.

Indexed as

AminopyridinesApoptosisAtaxia Telangiectasia Mutated ProteinsBenzamidesCell Line, TumorCell ProliferationCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p21G1 PhaseHistone Deacetylase InhibitorsHumansKiller Cells, NaturalLymphomaResting Phase, Cell CycleSignal TransductionTumor Suppressor Protein p53AminopyridinesAtaxia Telangiectasia Mutated ProteinsATM protein, humanBenzamidesCDKN1A protein, humanCheckpoint Kinase 2CHEK2 protein, humanCyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsN-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamideTP53 protein, humanTumor Suppressor Protein p53Cell cycle checkpoint pathwayChidamideDNA damage responseNK/T cell lymphoma

Identifiers

PMID29504068

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.